CV physiology

Question 1

IKAch current

Answer 1

Atrial tissues

Question 2

Where is Ito strongest

Answer 2

Atrial myocytes

Question 3

Role of late Na+ currents

Answer 3

Inward rectifiers, plateau
Outward currents

Question 4

IKur

Answer 4

Ultra rapid K+ current in atrial myocytes

Question 5

IK1

Answer 5

Voltage regulated, prominent in ventricles

Question 6

IK ATP

Answer 6

activated by ADP, inhibited by ATP

Question 7

Role of outward rectifiers currents

Answer 7

repolarizing

Question 8

Types of K+ channels

Answer 8

Inward rectifiers: IK1, IK Ach, IK ATP (ischemia)

Delayed rectifiers outward currents: IKur, IKr, IKs

Transient outwards: Ito

Question 9

Which current is associated w/ QT prolongation w/ drugs

Answer 9

IKr

Question 10

Rectification

Answer 10

direction of positive ion movement across membrane

Inward rectification: near cell RMP

Question 11

What affects inward rectification currents

Answer 11

Near RMP
HyperK+
Vagal tone
Ischemia

Question 12

ECG manifestation of K+current

Answer 12

Ito
J wave

Question 13

Inherited channelopathies

Answer 13

QT prolongation
KCNQ1: eng springer spaniels

Arrhythmias and SD

Question 14

Effect of ionophores

Answer 14

Transport ions across cell membranes = myocardial injury (poison cell) in horses and camelids

Question 15

Factors affecting HR (channels)

Answer 15

Alteration of minimal diastolic potential:
incr If, IK1
Blockage of current stim: If, ICaL
metabolic state: incr IKATP, temperature, thyroid

Question 16

Effects of autonomic system of SA node control

Answer 16

Symp: stim IF, ICaL
psymp: incr IKAch and incr Gi

Question 17

Therapeuthic targets for SA node control

Answer 17

Affect IF and ICaL: diltiazem and ivabradine
Indirectly affect currents by blockng B or M2 receptors

Question 18

Membrane clock

Answer 18

long and short lasting currents

Question 19

Ca2+ clock

Answer 19

Ca cycling changes of intracell Ca2+

Question 20

Effect of vagal stimulation

Answer 20

Decrease HR = open IKach and inhibit Ca2+ influx = depress AV and SA node
Shortens AP

Question 21

Clinical indications of ivabradine

Answer 21

Decrease HR: MS
Junctional tachy: labs

Question 22

Anti arrhythmic classification class 0

Answer 22

Funny channel blockers
Hyperpolarization activated cyclic nucleotide gated

Ivabradine

Question 23

Anti arrhythmic classification class Ia

Answer 23

Na+ channel blockers
INTERmediate dissociation
+ some effects on K+ channels

Quinidine, Disopyramide, Procainamide, Ajmaline

Question 24

Anti arrhythmic classification class Ib

Answer 24

Na+ channel blockers
RAPID dissociation

Lidocaine, Mexiletine

Question 25

Anti arrhythmic classification class Ic

Answer 25

Na+ channel blockers SLOW dissociation Flecainide, Propafenone

Question 26

Anti arrhythmic classification class Id

Answer 26

selective for late Na+ channel current and atrial-selective peak Na channel Ranolazine

Question 27

Anti arrhythmic classification class II

Answer 27

Class IIa (beta-adrenergic blockers) * Nonselective: propranolol, carvedilol, nadolol * Selective: atenolol, esmolol, metoprolol, bisoprolol, betaxolol Class IIb (nonselective beta agonists) * Isoproterenol Class IIc (muscarinic M2 receptor inhibitors) * Atropine, hyoscine,[hyoscyamine sulfate], scopolamine Class IId (muscarinic M2 receptor activators) * Digoxin, carbachol, pilocarpine, methacholine Class IIe (adenosine A1 receptor activators) * Adenosine

Question 28

Anti arrhythmic classification class III

Answer 28

Class IIIa (voltage dependent K + channel blockers) * Sotalol, amiodarone, dronedarone * Dofetilide, ibutilide

Question 29

Anti arrhythmic classification class IV

Answer 29

Class IVa (surface membrane Ca ++ channel blockers) * Diltiazem, verapamil

Question 30

Regulation of actin and myosin interaction

Answer 30

tropomyosin (structural) troponin complex

Question 31

Role of TnC

Answer 31

Binds to Ca2+ Cradica specific biomarker

Question 32

Excitation contraction coupling events

Answer 32

Summary of Myocardial Cell Contraction (correlates to numbers) 1. Cell depolarizes (phase 0 of action potential) 2. Voltage change opens the long-lasting calcium channels 3. Extracellular calcium enters cytoplasm via L-type channels (Phase 2 of Action Potential) 4. Triggering extracellular Ca ++ releases more Ca ++ from the sarcoplasmic reticulum (SR) stores via the calcium release channel (ryanodine receptor) 5. Increased cytosolic calcium 6. Calcium binds to troponin (C) and Inhibition is removed: 7. ATP is hydrolyzed. 8. Actin & Myosin (heads) interact so that myofilaments “ratchet and slide” (crossbridge cycling) 9. Sarcomere tenses (isometrically) and then shortens (so the Z discs move towards each other) and with structural elements operative lead to myocardial contraction. 10. Ca ++ leaves cell (sodium-Ca ++ exchanger) & is re-sequestered in SR using the pump SERCA; The myocyte relaxes

Question 33

Effect of pimo on excitation contraction coupling

Answer 33

incr sensitivity of TnC for Ca2+